Post-cardiac arrest temperature manipulation alters early EEG bursting in rats.

Abstract

Hypothermia improves outcomes after cardiac arrest (CA), while hyperthermia worsens injury. EEG recovers through periodic bursting from isoelectricity after CA, the duration of which is associated with outcome in normothermia. We quantified burst frequency to study the effect of temperature on early EEG recovery after CA. Twenty-four rats were divided into three groups, based on 6h of hypothermia (T=33 degrees C), normothermia (T=37 degrees C), or hyperthermia (T=39 degrees C) immediately post-resuscitation from 7-min asphyxial CA. Temperature was maintained using surface cooling and re-warming. Neurological recovery was defined by 72-h neurological deficit score (NDS). Burst frequency was higher during the first 90min in rats treated with hypothermia (25.6+/-12.2min(-1)) and hyperthermia (22.6+/-8.3min(-1)) compared to normothermia (16.9+/-8.5min(-1)) (p<0.001). Burst frequency correlated strongly with 72-h NDS in normothermic rats (p<0.05) but not in hypothermic or hyperthermic rats. The 72-h NDS of the hypothermia group (74, 61-74; median, 25-75th percentile) was significantly higher than the normothermia (49, 47-61) and hyperthermia (43, 0-50) groups (p<0.001). In normothermic rats resuscitated from CA, early EEG burst frequency is strongly associated with neurological recovery. Increased bursting followed by earlier restitution of continuous EEG activity with hypothermia may represent enhanced recovery, while heightened metabolic rate and worsening secondary injury is likely in the hyperthermia group. These factors may confound use of early burst frequency for outcome prediction.